**2. Atherosclerotic plaque morphology**

Atherosclerotic plaques are not static lesions; they undergo dynamic changes in their size and morphological characteristics. These changes manifest themselves as changes in plaque volume and consistency, otherwise known as *plaque progression* and *regression*. These, together with adaptive responses of the arterial wall, determine the degree of stenosis in the diseased artery. [10-12] This degree of stenosis is the measurable clinical finding which, together with timing and nature of symptoms and co-morbidities, correlates with the risk of developing further neurological events. [13]

Other researchers have found a definite increase in the incidence of plaque ulceration in patients with symptomatic carotid artery disease. Most notably, following review of 593 angiograms in the North American Symptomatic Carotid Endarterectomy Trial (NASCET), 34 percent of medically treated patients were found to have ulcerated plaques with reasonable certainty; this figure was 36 percent for those assigned to surgery. At 2 years, 30 percent of the medically treated group with ulceration had suffered a non-fatal stroke or vascular death

Carotid Plaque Morphology: Plaque Instability and Correlation with Development of Ischaemic Neurological Events

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One reason for this difference may be the time interval between the duration of symptoms and surgery in some of the studies. Lusby *et al* reported re-endothelialisation of several plaques, and suggested that this is particularly likely when the time span between the onset of symp‐

The strength of the evidence from the NASCET trial has meant that most clinicians recognise plaque cap ulceration as a risk factor for development of further carotid territory embolic neurological events. Preoperative evidence of plaque cap ulceration has been included in

The raised lesion or fibro-lipid plaque is the archetypal lesion of atherosclerosis and compli‐ cations of this lesion (fissure and ulceration) form the basis of the vast majority of cases of occlusive arterial disease. All atherosclerotic plaques share two basic morphological compo‐

*Fibrous cap:* a thick layer of fibrous connective tissue, which is significantly thicker and much less cellular than the normal intima and contains lipid-filled macrophages, collagen and

*Atheroma:* A necrotic mass of lipid that forms the core of the lesion. Loss of continuity of the endothelium is the main step in the progression of a plaque and increases the permeability of the intima to lipoproteins, permits platelet-vessel wall interaction and release of growth factors

Leahy demonstrated that various elements of the plaque are available as potential emboli. [20] This includes the fibrous cap overlying complex plaques, the contents that include cholesterol crystals, the breakdown products of intra-plaque haemorrhage, and fibrous or cartilaginous material as well as calcified tissue. Hollenhorst showed the presence of cholesterol emboli in the retinal artery of patients suffering from amaurosis fugax, in the form of bright plaques that were seen in the extra-cranial carotid vessels. [21] Bock *et al* reported that soft plaques (lipid laden and haemorrhagic plaque) behave in an unstable way and tend to ulcerate, whilst fibrous

Based on the natural history and pathological changes within the plaque the American Heart Association (AHA) has classified atherosclerotic lesions [23] (table 1). This classification that

compared to only 17 percent of those without plaque ulceration [17].

stroke risk calculators such as the Oxford Stroke Risk calculator. [19]

toms and endarterectomy exceeds 3 weeks. [18]

**4. Composition of an atherosclerotic plaque**

leading to formation of thrombus on the vessel wall.

or calcified plaques behave differently. [22]

nents:

smooth muscle cells;

Over the last 20 years a lot has been learned about the morphological characteristics of an atherosclerotic plaque responsible for plaque progression and instability. [10-12] Morpholog‐ ical characteristics of atherosclerotic plaques can be discussed in the context of plaque surface characteristics and the composition of the atherosclerotic lesion.

There has been conflicting evidence regarding the significance of plaque 

*al* did not find any significant difference in the incidence of ulceration between 

#### **3. Plaque surface characteristics** ulceration in the evolution of symptomatic disease. In a large study, Imparato *et*

Julian *et al* in 1963 were the first to discuss the issue of carotid plaque ulceration. They reported 17 cases of macroscopic plaque ulceration with thrombosis in the ulcer crater and suggested this as a source for embolisation. [12] Ulceration has been described as an observable disruption of intima exposing the adjacent atheromatous plaque or media [13] (figure 1). symptomatic and asymptomatic groups.14‐16 

**Figure-1: A carotid endarterectomy specimen containing a large ulcer which is associated with intra-plaque haemorrhage.** There has been conflicting evidence regarding the significance of plaque ulceration in the evolution of symptomatic disease. In a large study, Imparato *et al* did not find any significant difference in the incidence of ulceration between symptomatic and asymptomatic groups. [14-16]

Other researchers have found a definite increase in the incidence of plaque ulceration in patients with symptomatic carotid artery disease. Most notably, following review of 593 angiograms in the North American Symptomatic Carotid Endarterectomy Trial (NASCET), 34 percent of medically treated patients were found to have ulcerated plaques with reasonable certainty; this figure was 36 percent for those assigned to surgery. At 2 years, 30 percent of the medically treated group with ulceration had suffered a non-fatal stroke or vascular death compared to only 17 percent of those without plaque ulceration [17].

One reason for this difference may be the time interval between the duration of symptoms and surgery in some of the studies. Lusby *et al* reported re-endothelialisation of several plaques, and suggested that this is particularly likely when the time span between the onset of symp‐ toms and endarterectomy exceeds 3 weeks. [18]

The strength of the evidence from the NASCET trial has meant that most clinicians recognise plaque cap ulceration as a risk factor for development of further carotid territory embolic neurological events. Preoperative evidence of plaque cap ulceration has been included in stroke risk calculators such as the Oxford Stroke Risk calculator. [19]
